Epithelial ovarian cancer is the deadliest cancer of the female reproductive tract. Currently, there is neither a reliable means for early detection nor very efficient treatment options. Genetic lesions that have a major etiological role in sporadic and familial ovarian carcinogenesis include activating K-RAS mutations (K-RASG12D) and loss-of-function p53, PTEN, and BRCA1 mutations. The main goal of this proposal is to characterize the mouse models of endometriosis and endometrioid ovarian cancer that I recently developed. These studies will allow me to evaluate the pathogenetic links between endometriosis and endometrioid ovarian cancer. Furthermore, the analysis of these models will make possible the identification of new therapeutic targets. Finally, they will allow the screening of future therapeutic and chemopreventive agents in a relevant in vivo context.